1. Field of the Invention
This invention relates generally to methods of diagnosis, evaluation, or treatment of tissue, and more particularly, to methods of utilizing voltage gradient mapping to determine the locations of relevant portions of cardiac tissue for ablative therapy.
2. Background
Atrioventricular nodal reentry tachycardia (AVNRT) is the most common supraventricular tachycardia inducible in the electrophysiology lab (See, e.g., Bastani et al., “Acute and long-term outcome of cryoablation therapy of typical atrioventricular nodal reentrant tachycardia,” Europace, 2009 August (8):1077-82; Estner et al., “Acute and long-term results of slow pathway ablation in patients with atrioventricular nodal re-entrant tachycardia—an analysis of the predictive factors for arrhythmia recurrence,” Pacing Clin. Electrophysiol, 28:102-10). Since the early 1990's, ablative therapy has proven to be the treatment of choice, beginning with radiofrequency application and more recently cryoablation (See, e.g., Bastani et al.; Fazekas et al., “Treatment of AV-nodal reentry tachycardia by transcatheter radiofrequency ablation,” Orv Hetil, 1994 Aug. 20; 135 (34):1853-7). Although the procedure is highly successful with a relatively low complication rate, both complications and unsuccessful procedures remain. Successful ablations are seen in 91% to 99% of patients, with recurrence seen in 5-9% and heart block 1% (See, e.g., Bastani et al.; Zrenner et al., “Transvenous cryoablation versus radiofrequency ablation of the slow pathway for the treatment of atrioventricular nodal re-entrant tachycardia: a prospective randomized pilot study,” Eur. Heart J. 2004, 25:2226-31; Silver et al., “Cryoablation of atrioventricular nodal reentrant tachycardia with an 8 mm-tip cryocatheter in pediatric patients: an early experience,” Heart Rhythm Society, Scientific Sessions abstract (2008); Clague et al., “Targeting the slow pathway for atrioventricular nodal reentrant tachycardia: initial results and long-term follow-up in 379 consecutive patients,” Eur. Heart J., 2001 January, 22 (1):82 (2001); Chan et al., “Treatment of atrioventricular nodal re-entrant tachycardia by cryoablation with a 6 mm-tip catheter vs. radiofrequency ablation,” Europace, 2009 August, 11 (8):1065-70). There is a higher chance of recurrence in patients with single AV nodal echo versus patients with complete elimination of the slow pathway at the end of the procedure (See, e.g., Bastani et al.; Estner et al.; Manolis et al., “Radiofrequency ablation of slow pathway in patients with atrioventricular nodal reentrant tachycardia. Do arrhythmia recurrences correlate with persistent slow pathway conduction or site of successful ablation?”, Circulation, 1994, 90:2815-19; Baker et al., “Predictors of recurrent atrioventricular nodal reentry after selective slow pathway ablation,” Am. J. Cardiol. 1994, 73:765-9; Silva et al., “Relationship between conduction persistence through the slow pathway after atrioventricular nodal reentry tachycardia radiofrequency ablation and its recurrence,” Arq. Bras. Cardiol. 1998, 71:117-20; Gupta et al., “Cryoablation compared with radiofrequency ablation for atrioventricular nodal re-entrant tachycardia: analysis of factors contributing to acute and follow-up outcome,” Europace, 2006, 8:1022-6). Additionally, multiple AV nodal pathways are observed in approximately 39% of patients with AVNRT (See, e.g., Heinroth et al., “Multiple AV nodal pathways in patients with AV nodal reentrant tachycardia—more common than expected?”, Europace, 2002 October, 4 (4):375-82; Tai et al., “Multiple anterograde atrioventricular node pathways in patients with atrioventricular node reentrant tachycardia,” J. Am. Coll. Cardiol. 1996, 28:725-31).
Successful slow pathway ablation has previously been based primarily on anatomic and electrophysiological characteristics. The slow pathway has been described as being located along the inferior aspect of Koch's Triangle (see FIG. 1A), toward the tricuspid valve with an atrial voltage ratio 1/10th to ½ that of the ventricular voltage (See, e.g., Fazekas et al.; Haissaguerre et al., “Elimination of atrioventricular nodal reentrant tachycardia using discrete slow potentials to guide application of radiofrequency energy,” Circulation, 1992, 85:164-74; Medkour et al., “Anatomic and Functional Characteristics of a Slow Posterior AV Nodal Pathway: Role in Dual-Pathway Physiology and reentry,” Circulation 1998, 98:164-74; Kalbfleisch et al., “Randomized comparison of anatomic and electrogram mapping approaches to ablation of the slow pathway of atrioventricular node reentrant tachycardia,” J. Am. Coll. Cardiol. 1994, 23:716-23; Manolis et al, “Arrhythmia recurrences are rare when the site of radiofrequency ablation of the slow pathway is medial or anterior to the coronary sinus os,” Europace, 2002, 4:193-9; Wathen et al., “An anatomically guided approach to atrioventricular node slow pathway ablation,” Am. J. Cardiol. 1992, 70 (9):886-9). Ablative therapy is applied in the region of the slow pathway until either a junctional response is produced (RF energy), or non-inducibility with, or without, AV Nodal echo beats results (cryoablation or RF energy) (See, e.g., Friedman H. L., “How to ablate atrioventricular nodal reentry using cryoenergy,” Heart Rhythm, 2005, 2:893-6; Stabile et al., “The predictive value of junctional beats during the radiofrequency transcatheter ablation of the slow pathway of the nodal reentry circuit,” G. Ital. Cardiol. 1999, 29:549-54; De Sisti et al., “Transvenous cryo-ablation of the slow pathway for the treatment of atrioventricular nodal reentrant tachycardia: a single-centre initial experience study,” Europace, 2007, 9:401-6; Jentzer et al., “Analysis of junctional ectopy during radiofrequency ablation of the slow pathway in patients with atrioventricular nodal reentrant tachycardia,” Circulation 1994, 90:2820-6; Iakobishvili et al., “Junctional rhythm quantity and duration during slow pathway radiofrequency ablation in patients with atrioventricular nodal re-entry supraventricular tachycardia,” Europace 2006, 8:588-91). If the ablation lesion was unsuccessful, the catheter is repositioned, superiorly toward the AV Nodal region and the His catheter. Success is measured by the inability to induce AVNRT and/or a change in AV nodal properties (induction of a single echo beat) with an isuprel infusion (See, e.g., Weismüller et al., “Is electrical stimulation during administration of catecholamines required for the evaluation of success after ablation of atrioventricular node re-entrant tachycardias?”, J. Am. Coll. Cardiol., 2002, 39:689-94. Unfortunately, in some patients, both anatomic and electrophysiologic criteria may not be sufficient. In such patients, ablations may become prolonged and may have a greater potential for failure or complication.
A number of approaches have been suggested for ablative treatment of atrial fibrillation. Either an anatomic based therapy, focused primarily upon isolation of the pulmonary veins, or targeted ablation of high frequency regions has been reported to have moderate success in paroxysmal and modest success in chronic atrial fibrillation. Because of the chaotic nature of the arrhythmia, conventional activation mapping has not proved helpful. Therefore the reasons for success or failure have remained obscure.